The mechanisms which contribute to myocardial dysfunction in the Syrian Hamster with an hereditary cardiomyopathy are being pursued collaboratively in four medical centers using this common animal model. At the Albert Einstein College of Medicine, electron microscopic methods (S. Factor and E. Sonnenblick) are being used to define the ultrastructural changes that occur with time in the course of the disease. Using methods for the direct visualization of sarcomere shortening, contractile properties of the myocardium are being studied (J. Krueger). Electrophysiological properties (R. Aronson) are also being defined. The properties of purified contractile proteins are being studied to define reasons for decreased myosin ATPase activity and the effects of myosin bound proteases on this process (A. Bhan and J. Scheur). At the Medical College of Virginia (W. Weglicki and D. Pang) purified cell membranes and subcellular organelles are being studied. And, at the University of Toronto (M.Sole), abnormalities in catecholamine metabolism have been defined and altered sympathetic nervous system function is being explored. Increased synthesis of norepinephrine in nerve endings in the heart has been found. Central nervous system changes are now being fruitfully studied. Further, alterations in nuclear histone, metabolism have been noted and are being pursued.